To cite several examples, we note that the cytokine IL-6 is both necessary for Th17 differentiation and a known inhibitor of Treg maturation. Similarly, mature Th17 cells secrete IL17, which appears to have an inhibitory action on Treg cells. Likewise, the cytokine IL-2 seems to be necessary for the development of induced Treg cells, while at the same time inhibiting Th17 cell differentiation. Finally, it appears that the transcription factors for both Th17 cells and Treg cells can bind to each other, thereby antagonizing one another even further and leading to proliferation of either one cell type or the other, but not both. The interactions between Th17 cells and Treg cells outlined above are captured using the following set of three equations. As will be shown in the remainder of the paper, the Cianidanol dynamic interactions between Th17 cells and Treg cells enable the immune system to encode time-dependent information into relative T-cell population sizes. As these population sizes change through T-cell interactions with APCs and each other, the immune system comes to a final immunoregulatory decision by amassing either a large excess of Treg cells, in which case the immune system develops peripheral tolerance towards the antigen, or else a large excess of Th17 cells, in which case a defensive immune response is initiated. Before we move on to consider potential antigenic stimulation scenarios and their effects on the GDP decision-making process, we will first point out the general scope of the GDP model The purpose of this model is not to elucidate immune system operation in its entirety. Rather, GDP accounts for the Protocatechualdehyde fundamental ��on/off�� decision that the immune system must make regarding its response to a particular antigen. As a result, we do not use the GDP model to consider interactions with additional types of effector cells, nor do we attempt to relate our predictions to the specific ��variety�� of immune response that is mounted. Similarly, we do not discuss the steps leading from activation of an immune response to the development of memory cells primed for a subsequent encounter with the stimulating pathogen.